Evidence map›Paper›PMID 18026184›Full record

ArticleProstate cancer and prostatic diseases2008

NAT2 and NER genetic variants and sporadic prostate cancer susceptibility in African Americans.

S Hooker, C Bonilla, F Akereyeni, C Ahaghotu, R A Kittles

Abstract read
PubMed Publisher
In one paragraph

Article in Prostate cancer and prostatic diseases, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 6 pooled it
1.2field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 6 syntheses or guidelines pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Aging · 2018
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Article
  8. Review
  9. Polymorphisms inJournal of Cancer · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

S HookerSection of Genetic Medicine, Department of Medicine, Pritzker School of Medicine, The University of Chicago, Chicago, IL 60637, USA.
C Bonilla
F Akereyeni
C Ahaghotu
R A Kittles
Howard University · USUniversity of Chicago · USUniversity of Oxford · GB

Funding

The Howard University SCORE Program Supplemental GrantS06GM008016 · NIGMS · HOWARD UNIVERSITY · PI NELSON, KAREN ELIZABETH · 1989 to 2009
$16.1M
NIGMS NIH HHS S06GM08016
6 · The paper itself

Abstract

Prostate cancer is a common malignancy that disproportionately affects African-American men. Environmental factors and variation in genes responsible for chemical and dietary carcinogen metabolism and DNA damage repair may modulate risk. Fourteen single nucleotide polymorphisms in NAT2 and four NER genes (ERCC1, XPF/ERCC4, XPG/ERCC5 and CSB/ERCC6) were genotyped in a case-control study of 254 African-American prostate cancer cases and 301 healthy controls from Washington, DC. Smoking status, BMI, age and genetic ancestry were included as covariates in the association analyses. We found that individuals homozygous for the XPG/ERCC5 -72C/T promoter polymorphism had a significant reduction in risk, for prostate cancer (OR=0.12; 95% CI=0.03-0.48). A haplotype trend regression test also revealed a protective effect for the haplotype bearing the T allele (P=0.003). In silica analyses suggest a functional implication for the promoter variant since it deletes a GCF transcriptional factor-binding site responsible for the downregulation of transcription. The protective effect of the promoter SNP on risk for prostate cancer was independent of smoking. In contrast, none of the SNPs typed for NAT2, ERCC1, ERCC4 and ERCC6 showed significant association with risk. Additional tests for genotype interactions were not significant. We note that there may be other factors, such as dietary exposures, which may modulate prostate cancer risk in combination with genetic variation within the NAT2 and NER genes. Our results, in combination with previous observations of LOH for ERCC5 in prostate tumors, provide further evidence for a role of XPG/ERCC5 in the etiology of prostate cancer.

Indexed as

AdultAgedAged, 80 and overAllelesArylamine N-AcetyltransferaseBlack or African AmericanGenetic MarkersGenetic Predisposition to DiseaseGenotypeHealthHumansLiver X ReceptorsMaleMiddle AgedOrphan Nuclear ReceptorsPolymorphism, Single NucleotideArylamine N-AcetyltransferaseGenetic MarkersLiver X ReceptorsNAT2 protein, humanOrphan Nuclear ReceptorsReceptors, Cytoplasmic and Nuclear

Identifiers

PMID18026184
OpenAlexW2060300572

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.